Atrial Fibrillation: Management
Strategies In The Emergency
Department
Abstract
February 2013
Volume 15, Number 2
Authors
Marisa L. Oishi, MD, MPH
Attending Physician, Department of Emergency Medicine, Weill
Medical College of Cornell University, The Brooklyn Hospital Center,
Brooklyn, NY; Adjunct Instructor, Department of Emergency Medicine,
Mount Sinai School of Medicine, New York, NY
Shelly Xing, MD
Atrial fibrillation and atrial flutter are the most common dysrhythmias seen in the emergency department. As the aging population
continues to grow, atrial fibrillation and atrial flutter are expected
to affect 6 million people by 2050. This will lead to an increase in
emergency department visits for symptoms from the disease itself
or its complications, such as heart failure or thromboembolic disease. This review examines the recent literature on the diagnosis
and management of atrial fibrillation. Evidence-based recommendations are provided, including cost-effective strategies to evaluate
new-onset arrhythmias and unstable patients with atrial fibrillation, rate control strategies, the use of medical and direct current
cardioversion for new-onset atrial fibrillation/atrial flutter, whom
and when to anticoagulate, and the use of the novel anticoagulation agents.
Department of Emergency Medicine, Weill Medical College of Cornell
University, The Brooklyn Hospital Center, Brooklyn, NY
Peer Reviewers
William J. Brady, MD
Professor of Emergency Medicine and Medicine, Chair, Medical
Emergency Response Committee, Medical Director, Emergency
Management, University of Virginia Medical Center, Charlottesville, VA
Keith A. Marill, MD
Assistant Professor, Harvard Medical School; Emergency Department
Attending Physician, Massachusetts General Hospital, Boston, MA
CME Objectives
Upon completing the article, you should be able to:
1.
Discuss the initial evaluation in patients with new-onset AF.
2.
Understand the common rate and rhythm controlling agents.
3.
Be familiar with the indication and contraindications for ED
cardioconversion.
4.
Differentiate among the different anticoagulation options and
when it is appropriate to start anticoagulation in the ED.
Prior to beginning this activity, see the back page for faculty
disclosures and CME accreditation information.
Editor-in-Chief
Corey M. Slovis, MD, FACP, FACEP
International Editors
Professor and Chair, Department
Peter Cameron, MD
of Emergency Medicine, Vanderbilt
Academic Director, The Alfred
University Medical Center; Medical
Emergency and Trauma Centre,
Director, Nashville Fire Department and
Monash University, Melbourne,
International Airport, Nashville, TN
Charles V. Pollack, Jr., MA, MD,
Australia
Steven A. Godwin, MD, FACEP
FACEP
Stephen H. Thomas, MD, MPH
Editorial Board
Professor and Chair, Department
Giorgio Carbone, MD
Chairman, Department of Emergency George Kaiser Family Foundation
William J. Brady, MD
of Emergency Medicine, Assistant
Chief, Department of Emergency
Medicine, Pennsylvania Hospital,
Professor & Chair, Department of
Professor of Emergency Medicine
Dean, Simulation Education,
Medicine Ospedale Gradenigo,
University of Pennsylvania Health
Emergency Medicine, University of
and Medicine, Chair, Medical
University of Florida COMTorino, Italy
System, Philadelphia, PA
Oklahoma
School
of
Community
Emergency Response Committee,
Jacksonville, Jacksonville, FL
Medicine, Tulsa, OK
Amin Antoine Kazzi, MD, FAAEM
Michael S. Radeos, MD, MPH
Medical Director, Emergency
Associate Professor and Vice Chair,
Gregory L. Henry, MD, FACEP
Assistant Professor of Emergency
Management, University of Virginia
Jenny Walker, MD, MPH, MSW
Department of Emergency Medicine,
CEO, Medical Practice Risk
Medicine, Weill Medical College
Medical Center, Charlottesville, VA
Assistant Professor, Departments of
University of California, Irvine;
Assessment, Inc.; Clinical Professor
of Cornell University, New York;
Preventive Medicine, Pediatrics, and
Peter DeBlieux, MD American University, Beirut, Lebanon
of Emergency Medicine, University of
Research Director, Department of
Medicine Course Director, Mount
Professor of Clinical Medicine,
Michigan, Ann Arbor, MI
Emergency Medicine, New York
Sinai Medical Center, New York, NY
Hugo Peralta, MD
Interim Public Hospital Director
Hospital Queens, Flushing, New York
John M. Howell, MD, FACEP
Chair of Emergency Services,
of Emergency Medicine Services,
Ron M. Walls, MD
Clinical Professor of Emergency
Hospital Italiano, Buenos Aires,
Robert L. Rogers, MD, FACEP,
Emergency Medicine Director of
Professor and Chair, Department of
Medicine,
George
Washington
Argentina
FAAEM,
FACP
Faculty and Resident Development,
Emergency Medicine, Brigham and
University, Washington, DC; Director
Assistant Professor of Emergency
Louisiana State University Health
Women’s Hospital, Harvard Medical Dhanadol Rojanasarntikul, MD
of Academic Affairs, Best Practices,
Medicine, The University of
Science Center, New Orleans, LA
School, Boston, MA
Attending Physician, Emergency
Inc, Inova Fairfax Hospital, Falls
Maryland School of Medicine,
Medicine, King Chulalongkorn
Francis M. Fesmire, MD, FACEP
Scott Weingart, MD, FACEP
Church, VA
Baltimore, MD
Memorial Hospital, Thai Red Cross,
Professor and Director of Clinical
Associate Professor of Emergency
Thailand; Faculty of Medicine,
Alfred Sacchetti, MD, FACEP
Research, Department of Emergency Shkelzen Hoxhaj, MD, MPH, MBA
Medicine, Mount Sinai School of
Chulalongkorn University, Thailand
Chief of Emergency Medicine, Baylor
Assistant Clinical Professor,
Medicine, UT College of Medicine,
Medicine; Director of Emergency
College
of
Medicine,
Houston,
TX
Department of Emergency Medicine, Critical Care, Elmhurst Hospital
Chattanooga; Director of Chest Pain
Suzanne Peeters, MD
Thomas
Jefferson
University,
Center, Erlanger Medical Center,
Center,
New
York,
NY
Emergency Medicine Residency
Eric Legome, MD
Philadelphia, PA
Chattanooga, TN
Director, Haga Hospital, The Hague,
Chief of Emergency Medicine,
Senior
Research
Editor
The Netherlands
King’s
County
Hospital;
Professor
of
Scott Silvers, MD, FACEP
Nicholas Genes, MD, PhD
Joseph D. Toscano, MD
Clinical
Emergency
Medicine,
SUNY
Chair,
Department
of
Emergency
Assistant Professor, Department of
Emergency Physician, Department
Downstate College of Medicine,
Medicine, Mayo Clinic, Jacksonville, FL
Emergency Medicine, Mount Sinai
of Emergency Medicine, San Ramon
Brooklyn, NY
School of Medicine, New York, NY
Regional Medical Center, San
Ramon, CA
Andy Jagoda, MD, FACEP
Professor and Chair, Department of
Emergency Medicine, Mount Sinai
School of Medicine; Medical Director,
Mount Sinai Hospital, New York, NY
Michael A. Gibbs, MD, FACEP
Professor and Chair, Department
of Emergency Medicine, Carolinas
Medical Center, University of North
Carolina School of Medicine, Chapel
Hill, NC
Keith A. Marill, MD
Assistant Professor, Harvard Medical
School; Emergency Department
Attending Physician, Massachusetts
General Hospital, Boston, MA
Case Presentations
Critical Appraisal Of The Literature
You have just arrived to your morning shift in the ED,
and as you are about to sit down for a cup of coffee, a
37-year-old female presents, complaining of palpitations
that started this morning. She has no past medical history, is on no medications, and denies any drug use. On
physical exam, she is slightly uncomfortable, has an irregular heart rate of 190 beats/min, and has a blood pressure
of 115/75 mm Hg. Her ECG shows rapid atrial fibrillation
with wide, bizarre QRS complexes. You wonder what
the origin of the dysrhythmia is and whether you should
rate control the patient with diltiazem or whether there is
another intervention you are not thinking of . . . Two beds down, the nurse tells you about an 85-yearold male from a nursing home who is febrile to 39.5°C, is
tachycardic with a heart rate of 160 beats/min, and has
a blood pressure of 98/57 mm Hg. He has a history of
dementia, diabetes, and hypertension and is nonverbal at
baseline. He is minimally responsive and unable to give
you additional information. You begin fluid resuscitating
him and administer acetaminophen, and you notice on the
monitor that his heart rhythm is irregular. You wonder
what the safest way to control the patient’s rhythm is and
whether and how he should be anticoagulated . . .
An Ovid MEDLINE® and a PubMed search were carried out for literature from 2002 through October 2012
using the search terms atrial fibrillation, atrial flutter,
management, treatment, and emergency. The Cochrane
Database of Systematic Reviews and the National
Guidelines Clearinghouse (www.guidelines.gov) were
also searched; 374 abstracts were identified, of which,
140 manuscripts were reviewed. In addition, the
bibliographies of all reviewed articles were reviewed
for additional publications. This process resulted in 10
practice guidelines, 10 systematic reviews, 69 prospective studies, and 35 retrospective studies.
The recommendations presented in this review were excerpted from the relevant guidelines
of the American College of Cardiology (ACC),
the American Heart Association (AHA), and the
European Society of Cardiology’s (ESC’s) “2006
Guidelines for the Management of Patients with
Atrial Fibrillation”8 and the 2011 American College of Cardiology Foundation (ACCF), AHA,
and Heart Rhythm Society’s “Focused Update on
the Management of Patients With Atrial Fibrillation.”9 These guidelines focus on both acute and
long-term management of AF. The AHA levels
and classes of evidence are expanded in Table 1.
Additional guidelines that served as an important
resource included the Canadian Cardiovascular
Society’s “Atrial Fibrillation Guidelines 2010:
Management of Recent-Onset Atrial Fibrillation
and Flutter in the Emergency Department,”10 the
“Focused 2012 Update of the Canadian Cardiovascular Society Atrial Fibrillation Guidelines: Recommendations for Stroke Prevention and Rate/
Rhythm Control,”11 and the ESC’s Task Force for
Introduction
Atrial fibrillation (AF) is the most common sustained
cardiac arrhythmia.1,2 Atrial flutter (AFL) is often associated with AF, and both of the conditions may occur in the same patient. The prevalence of AF/AFL
has been increasing steadily over the past 20 years,
and population estimates based on United States
Census data estimate that 3 million cases of AF/AFL
were documented in 2010 alone.3
Both AF and AFL are associated with increased
thromboembolic events and stroke severity.4,5 AF/
AFL pose a tremendous healthcare and economic
burden; a retrospective analysis of 2001 national
healthcare databases found that AF/AFL accounted
for approximately 350,000 hospitalizations, 5 million office visits, and 276,000 emergency department
(ED) visits,6 leading to over $6 billion in healthcare
expense annually.7
Patients with AF/AFL may have presentations
that range from asymptomatic to severe life-threatening episodes that include syncope, congestive
heart failure, cardiogenic shock, stroke, and myocardial infarction. The emergency clinician must be
alert to the diagnosis and understand the contributing factors and comorbidities. This issue of Emergency Medicine Practice provides an analysis of the best
available evidence regarding the management of
AF/AFL, including cardioversion, rate control, and
anticoagulation.
Emergency Medicine Practice © 20132
Table 1. American Heart Association
Classification Of Levels And Classes Of
Evidence9
Levels of Evidence
Level A
Multiple populations evaluated. Data derived from multiple randomized controlled trials or meta-analyses
Level B
Limited populations evaluated. Data derived from a
single randomized trial or nonrandomized studies
Level C
Very limited populations evaluated; only consensus
opinion of experts, case studies, or standard of care
Classes of Evidence
Class I
Benefit >>> Risk: procedure SHOULD be performed/
administered
Class IIa
Benefit >> Risk; IT IS REASONABLE to perform procedure/administer treatment
Class IIb
Benefit ≥ Risk; procedure/treatment MAY BE CONSIDERED
Class III
No proven benefit/harmful to patients
www.ebmedicine.net • February 2013
the Management of Atrial Fibrillation’s “Guidelines for the Management of Atrial Fibrillation.”2
als younger than 60 years of age without clinical or
echocardiographic evidence of cardiopulmonary
disease (including hypertension),35 and it carries
favorable risk profiles in regard to thromboembolism and mortality. Nonvalvular AF refers to AF in
individuals without rheumatic mitral valve disease,
prosthetic heart valves, or valve repair.
Epidemiology
Estimates of AF/AFL prevalence have been reported
to be 1% to 4% in the general population and 9%
in patients over the age of 80.12,13 The incidence of
AF/AFL increases with age, and it is more common
among males, with a median age of onset of 66.8
years for men and 74.6 years for women.14 AFL has
been studied much less as a clinically separate entity,
but estimates suggest that the incidence of AFL is 88
per 100,000 person-years and that there are roughly
200,000 new cases of AFL in the United States annually.15 The incidence rate for AF has shown to vary
by age, from < 0.5 per 1000 person-years before age
50 to as high as 20.7 per 1000 person-years among
those 80 to 84 years of age.16-18 As the population
ages, studies suggest that AF/AFL will affect 6 million people by 2050.19
Pathophysiology
AF and AFL are supraventricular tachycardias that
arise from disorganized or abnormal atrial depolarization. Atrial fibrosis and loss of atrial muscle mass
are the most frequent histopathological changes in
AF. Electrical remodeling occurs, resulting in multiple reentry circuits or rapidly firing atrial foci and
shortening of atrial refractoriness and action potential, thus contributing to the maintenance of AF.8
Triggers for AF include autonomic nervous system
stimulation, bradycardia, atrial premature beats or
tachycardia, accessory atrioventricular pathways,
ectopic foci occurring in the sleeves of atrial tissues
within the pulmonary veins or vena caval junctions,
and atrial stretch.36
Decreased atrial contractile function and loss of
synchronous atrial activity (“atrial kick”) combined
with rapid ventricular responses may have hemodynamic consequences with a markedly decreased
cardiac output.37,38 A persistently elevated ventricular rate during AF (usually > 120 beats/min) for
prolonged time periods may also result in increased
mitral regurgitation, eventually leading to a dilated
ventricular cardiomyopathy (tachycardia-induced
cardiomyopathy).39,40
Prolonged AF makes restoration and maintenance of sinus rhythm more difficult, as the adage
“atrial fibrillation begets atrial fibrillation” suggests.
Repeated or prolonged episodes of AF result in
shortened effective refractory periods as electrophysiological remodeling occurs, which, combined
with increased atrial mass volume and delayed
conduction, favors sustained AF.8 Prolonged AF also
disturbs atrial contractile function, which may not
recover for days or weeks following the restoration
of sinus rhythm (“atrial stunning”), which has important implications for the duration of anticoagulation after cardioversion.
Etiology And Risk Factor Stratification
Cardiac causes of AF/AFL, as described in the Framingham Heart Study, include mitral valve disease,
myocardial disease, conduction system disorders,
Wolff-Parkinson-White syndrome, and pericardial
disease.13 Conditions associated with AF include
thyrotoxicosis, hypothermia, alcohol use, severe infection, hypoxia, pulmonary emboli and pneumonia,
kidney disease, obesity, diabetes mellitus, digoxin
toxicity, and electrolyte abnormalities.20-22 Intrathoracic surgery, such as cardiac or pulmonary surgery,
or invasive cardiac studies may also precipitate AF.23
AF is the most common cardiac complication of
hyperthyroidism, and it is estimated to occur in up
to 15% of hyperthyroidism patients;24,25 however,
hyperthyroidism accounts for < 1% of all patients
with new-onset AF.26
In the first 24 hours of myocardial infarction,
AF is common, and it carries a poor prognosis, with
higher 30-day, 6-month, and 1-year mortality and
stroke rates.27-29 The predicted incidence of myocardial infarction in patients with AF on presentation to
the ED is estimated to be as high as 5% to 15%.30-33
AF is categorized as follows:
• First detected episode
• Recurrent (after 2 or more episodes)
• Paroxysmal (if recurrent AF terminates spontaneously)
• Persistent (if sustained beyond 7 days)
Differential Diagnosis
AF/AFL are supraventricular tachycardias with the
distinguishing feature of unique P-wave morphologies.
AF has low-amplitude fibrillatory waves that result
in an irregularly irregular ventricular rhythm with an
absence of well-defined P-waves. AFL is characterized
by sawtooth-appearing P-waves with an atrial frequency around 300, often resulting in a regular ventricular
frequency around 75 or 150 beats/min, depending
Initial episodes of AF will often resolve spontaneously within 7 days, with most episodes selfterminating in < 24 hours. Persistent AF may require
termination via medications or direct current electric
cardioversion.34 Lone AF applies to AF in individuFebruary 2013 • www.ebmedicine.net
3
Emergency Medicine Practice © 2013
on the atrioventricular node conduction block. These
distinguishing characteristics may help differentiate AF
from other supraventricular tachycardias.
The wide QRS complexes in AF with WolffParkinson-White syndrome may give an appearance
similar to ventricular tachycardia; however, AF with
preexcitation can usually be distinguished by the
very rapid ventricular rate and irregularly irregular
rhythm. Table 2 presents the differential diagnosis
for patients suspected of having AF.
Prehospital Care
Prehospital care begins by assessing and stabilizing
the airway, breathing, and circulation. In hemodynamically stable patients, a targeted history and
physical examination should be performed to assess
for underlying causes of the tachycardia. According to the Advanced Cardiovascular Life Support
(ACLS) guidelines, cardioversion should be considered if the patient exhibits signs of hemodynamic
Table 2. Differential Diagnosis For Atrial
Fibrillation
Rhythm
Atrial Frequency, beats/min
Ventricular
Frequency,
beats/min
P-wave
Sinus tachycardia
100-180
100-180
Precedes
every QRS
complex
Atrial fibrillation
400-600
60-190,
irregularly
irregular
Absent
Atrial flutter
250-350
75-150,
regular,
sometimes
alternating
block
Sawtooth
Atrioventricular
nodal reentrant
tachycardia
180-250
180-250
In QRS
complex
(R)
Atrial tachycardia
120-250
75-250
Precedes
QRS;
P-wave
differs
from sinus
P-wave
Multifocal atrial
tachycardia
> 100
> 100
3 or more
different
P-wave
morphologies at
different
rates
Atrial fibrillation
with Wolff-Parkinson-White
syndrome
400-600
180-300, with
wide, bizarre QRS
complexes
Absent
Emergency Medicine Practice © 20134
compromise or poor coronary artery perfusion.43
The prehospital provider must consider that the
ACLS guidelines address patients with hemodynamic instability solely from acute AF/AFL. These
guidelines do not take into account the patient with
chronic AF/AFL who may be hemodynamically
unstable due to shock from another cause (such as
sepsis or hypovolemia), where interventions should
target the acute process.
There are few studies of prehospital management
of AF. One retrospective study of paramedic responses to 33 patients in rapid AF reported that optimal
prehospital care can be safely achieved with symptomatic treatment alone using nitroglycerine, furosemide, aspirin, and morphine. No adverse events were
reported; however, none of these patients were hemodynamically unstable.44 A small retrospective study
of 70 patients examining the safety of diltiazem in the
prehospital setting, and a case report of the Cardizem
Lyo-Ject® infusion for rapid AF found diltiazem to
safely decrease ventricular response to AF without
precipitating hypotension, endotracheal intubation,
cardiac arrest, or unstable dysrhythmias.45,46
Currently, there is no universally accepted treatment protocol for prehospital management of AF.
Initial management should be focused on providing
supportive care for the patient, with consideration
of crystalloid fluid boluses, intravenous (IV) diltiazem for rate control, or electrical cardioversion if the
patient becomes acutely unstable from AF/AFL.
Emergency Department Evaluation
History And Physical Examination
Presentation of AF/AFL may be related to the disease
itself or to complications from associated conditions
(eg, thromboembolism, heart failure, thyroid disease,
or alcohol or drug toxicity). Clinical symptoms associated with AF/ AFL may include anxiety, palpitations,
shortness of breath, dizziness, chest pain, or generalized fatigue. A careful history of medications and
alcohol and drug use should be obtained.
The physical examination must be comprehensive (with a full set of vital signs, including oxygen
saturation) and should include a careful evaluation
for evidence of thyroid disease (eg, exophthalmos
and enlarged thyroid) and for evidence of deep vein
thrombosis/pulmonary embolus (eg, unilateral
lower extremity swelling or tenderness). The cardiac
evaluation should assess rate, rhythm, and the presence of heart murmurs.
Diagnostic Studies
Electrocardiogram
The diagnosis of AF/AFL requires documentation of
an electrical heart tracing with at least a single lead
recording during the arrhythmia.
www.ebmedicine.net • February 2013
herbal products and supplements (such as creatine
monohydrate), especially young patients without
structural heart disease.52
Pregnancy tests should be obtained on women
of reproductive age, since pharmacological therapies
should be selected based on trimester of pregnancy.
Although AF is the most common dysrhythmia en-
Atrial Fibrillation Findings
Several characteristic electrocardiogram (ECG)
changes define AF:
1. Presence of low-amplitude fibrillatory waves on
ECG without defined P-waves
2. Irregularly irregular ventricular rhythm
3. Fibrillatory waves typically have a rate of > 300
beats per minute
4. Ventricular rate is typically between 100 and 160
beats per minute (See Figure 1)
Figure 1. Atrial Fibrillation With Rapid
Ventricular Response Around 150 Beats Per
Minute
Wolff-Parkinson-White syndrome (preexcitation
syndrome) should be considered in any patient with
bizarre, wide QRS complexes of different morphologies; in patients with a very rapid ventricular rate
with an RR interval > 250; and in younger patients
who present to the ED in AF. (See Figure 2.)
Atrial Flutter Findings
AFL is an atrial tachyarrhythmia secondary to a
reentry mechanism, and is characterized by an atrial
rate of 250 to 350 beats per minute. Ventricular rates
in AFL are usually around 150 beats per minute secondary to 2:1 conduction through the atrioventricular node. Classic ECG pattern includes the presence
of flutter waves. (See Figure 3.)
Note the irregularly irregular pattern with narrow-complex QRS complexes.
Figure 2. Atrial Fibrillation With WolffParkinson-White Preexcitation And
Conduction Through The Bypass Tract
Laboratory Tests
Initial laboratory testing is tailored to the patient’s
presentation. Tests to consider include a complete
blood cell count, metabolic panel, and hepatic function panel. Coagulation studies should be drawn
on patients, especially those on warfarin. A thyroid
panel is obtained for patients with clinical signs of
hyperthyroidism and in patients older than 55 with
new-onset AF,24 as older patients may not present
with classic signs and symptoms of hyperthyroidism.47,48 Thyroid function studies are also suggested
for the first episode of AF when the ventricular rate
is difficult to control.
This wide complex tachycardia with a rate of about 230 beats per minute looks similar to ventricular tachycardia; however, the “irregularly
irregular” rhythm and extremely rapid rate leads towards atrial fibrillation with preexcitation.
Cardiac Serum Markers
Cardiac serum markers may have some utility
in select patients suspected to be at risk of acute
coronary syndromes (ACS), including those with
ECG changes suspicious for ischemia or underlying
heart disease or significant risk factors for coronary
artery disease.31,49-51 Two studies that examined the
incidence of myocardial infarction among patients
admitted for AF found that 5% to 6% of patients
have an ACS.31,33 ST-segment elevation or depression > 2 mm on admission ECG were found to
be associated with patients diagnosed with acute
myocardial infarction.31
Figure 3. Atrial Flutter With 2:1 Block
Additional Studies
Urine drug screens may be obtained on a case-by-case
basis. Patients should be questioned about the use of
Figures 1-3 are reprinted with permission from: Nathanson L A, McClennen S, Safran C, Goldberger AL. ECG Wave-Maven: Self-Assessment Program for Students and Clinicians. http://ecg.bidmc.harvard.edu.
February 2013 • www.ebmedicine.net
The atrial rate is 320 with a 2:1 atrioventricular node conduction block
with a ventricular response of 160 beats per minute. The classic flutter “F” waves give a “sawtooth” appearance to the atrial activity.
5
Emergency Medicine Practice © 2013
countered in the ED, it is rare in pregnancy, and, when
encountered, it is usually associated with maternal hyperthyroidism, congenital heart disease, or rheumatic
heart disease.53 In this population, initial evaluation
should include ECG, basic laboratory tests, urine drug
screen, thyroid panel, and echocardiogram.54
Tests for underlying pulmonary embolism have
been suggested by some medical textbooks; however, most studies imply that patients who are otherwise not suspected of having pulmonary embolism
are unlikely to have pulmonary embolism and do
not require additional testing.55
Patients on digoxin (Lanoxin®, Cardoxin®,
Digitek®) should have their digoxin level obtained,
as noncompliance may result in rapid ventricular
response in those with chronic AF. Digoxin toxicity
may be associated with a variety of dysrhythmias,
including AF with a slow ventricular response. Digoxin toxicity is a relative contraindication to electrical cardioversion.
While theophylline (Uniphyl®, Elixophyllin®,
Theolair®) is rarely used today, toxicity is associated
with AF, and theophylline levels should be obtained
if the patient has been prescribed this drug.56
Imaging Studies
Chest radiography may be performed to evaluate
lung parenchyma and pulmonary vasculature for
significant findings such as pulmonary edema in
heart failure, pulmonary masses, left atrial enlargement from mitral valve regurgitation, Hampton
hump, or Westermark sign in pulmonary embolus.
Use of focused ultrasonography in hypotensive
patients with AF/AFL may help identify additional
causes of shock or hypotension.57-59 Cardiac views
can help to evaluate right heart strain that might
indicate a diagnosis of pulmonary embolism55 and
the presence of a pericardial effusion and cardiac
tamponade, and they may also assist in evaluating
left ventricular function. Measurement of the inferior
vena cava can assess intravascular volume depletion
and guide resuscitation.60,61 Additional views of the
abdominal aorta and the Morison pouch can help
eliminate causes of acute blood loss from occult aortic aneurysmal rupture or intraabdominal bleeding
as a cause of hypotension.58
Routine transthoracic echocardiography in the
ED is not recommended, but it may be performed
in the inpatient or outpatient setting to further
evaluate cardiac function and causative factors for
AF.12,62 Measurement of the left atrial size might also
help identify patients who might be successfully
converted and remain in normal sinus rhythm.63
Transesophageal echocardiography may help guide
acute cardioversion of patients with AF of unknown
duration, with evaluation of the atrial appendage for
clot visualization.8,64-70
Emergency Medicine Practice © 20136
Treatment Of Unstable Patients
Initial Approach To Management
The goals of AF management are focused on achieving hemodynamic stability, symptomatic treatment,
and the prevention of complications (such as thromboembolism).71,72 The initial management includes
cardiac monitoring, supplying supplemental oxygen
as needed, establishing IV access, and rapidly assessing the patient’s hemodynamic status. A history
and physical examination should be conducted,
with the focus placed on the duration and nature of
the symptoms, the comorbidities, and identifying
reversible causes of AF.
Emergent Stabilization Of Critically Ill
Patients
The 2010 ACLS guidelines suggest immediate direct
current cardioversion (DCC) for patients with altered
mental status, ischemic chest discomfort, acute heart
failure, hypotension, or other signs of shock or hemodynamic instability.43 Other patients who may benefit
from immediate DCC include those with wide complex AF/AFL that may signify an accessory pathway
with very rapid ventricular rates or hemodynamic
instability. These guidelines, however, do not address
many of the AF/AFL patients encountered in the
ED who are hemodynamically unstable due to other
disease processes (including sepsis, hypovolemia,
massive pulmonary embolism, or pericardial tamponade). Additionally, while the recommendations state
that cardioversion should be attempted in unstable
patients, the critically ill patient may have chronic
AF/AFL or additional comorbidities and illnesses
that may lead to failed or short-lived effects of DCC,
and alternative methods of stabilization must be considered early on. (See Table 3.)
For patients with AF/AFL who are hemodynamically unstable, initial actions to stabilize the patient
include obtaining large-bore intravascular access
and addressing intravascular volume depletion with
rapid infusions of 20- to 40-mL/kg crystalloid bolus
challenges.57 Concurrent evaluation for myocardial
infarction, signs of infection, or blood loss as a primary cause of hypotension should be conducted, and
initial therapies (including revascularization, early
goal-directed therapy, blood transfusion, and vasoactive agents, as warranted) should be targeted to the
underlying cause of hypotension or shock.
Electrical cardioversion may be the fastest method to obtain rate control in AF/AFL patients because
it converts the patient back to sinus rhythm; however,
it requires procedural sedation and carries a risk of
embolic events and cardiac arrhythmias. In unstable
patients without other causes for shock or hypotension and patients with preexcitation syndromes with
very rapid ventricular response, the use of DCC may
be life-saving, and it is the first-line treatment. For
www.ebmedicine.net • February 2013
these patients, emergent DCC should not be withheld
due to concerns for thromboembolism. Based on the new ACLS guidelines, the starting
energy for patients with AFL should be between 50
J and 100 J biphasic waveform synchronized cardioversion (or monophasic equivalent) and 100 J for AF;
however, a multicenter trial found that only 60% of
patients cardioverted with 100 J biphasic, while 90%
converted with 200 J.73 Thus, starting at a higher
energy may be beneficial in an unstable patient.73-75
(See Table 4.)
zem;83 however, none of the patients became hypotensive in either group.
Pretreatment Doses:
Phenylephrine
50-200 mcg every 1-2 minutes
Calcium
5-10 mL of calcium gluconate or
1-3 mL of calcium chloride
Rate-Control Agent Doses:
Amiodarone
150-mg bolus, then drip or repeat bolus
Diltiazem
2.5 mg/min continuous drip
until heart rate < 100 beats/min
(or 50-mg total dose)
Urgent Stabilization Of Hemodynamically
Unstable Patients
Rate-control medications will cause further hypotension in patients if they are given in the standard
recommended doses, but they may be necessary to
rate control a hemodynamically unstable patient
or a patient who fails emergent DCC (especially if
the AF/AFL is chronic). One strategy advocated to
reduce further hypotension includes pretreatment
with push-dose phenylephrine to a goal diastolic
blood pressure > 60 mm Hg prior to slow amiodarone or diltiazem infusion.76
Amiodarone lacks significant inotropic effects
and may have the added benefit of restoring sinus
rhythm.77 Low-dose diltiazem (< 0.2 mg/kg) was
shown in 1 small study to have less of a hypotensive effect on patients than standard-dose diltiazem;
however, none of the participants in this study were
hypotensive at baseline.78
Calcium, an inopressor, may have some beneficial effect as a pretreatment agent. Some studies
have shown that pretreatment with calcium may
reduce or reverse the hypotensive effects of verapamil.79-82 This was not shown in a trial with diltia-
Treatment Of Stable Patients
Treatment of hemodynamically stable patients focuses on symptom relief, maintenance of rate control
with consideration of cardioversion to sinus rhythm,
and the prevention of complications, such as thromboembolism.71,72
Selecting A Rate Control Versus A Rhythm
Control Strategy For Atrial Fibrillation/Atrial
Flutter
The acute ED management of AF/AFL is variable,
and few recommendations exist. The 2006 ACC/
AHA/ESC guidelines make no distinction between
ventricular rate and rhythm control management.
Multiple studies have shown no difference in allcause mortality, cardiovascular mortality, or stroke
rate among patients treated with rate or rhythm control;84-90 however, these studies did not investigate
the optimal management choice for new-onset AF/
AFL patients presenting to the ED.
Traditionally, most patients with new-onset AF
were rate-controlled with a beta blocker or calcium
channel blocker, admitted to the hospital, and subsequently converted to sinus rhythm or discharged
with rate control.91-93 Given the rising number of ED
visits for new-onset AF/AFL as well as increasing
pressures to decrease hospital admissions and total
hospital length of stay in order to reduce medical
costs and help alleviate ED crowding, there is growing interest in cardioversion of patients with newonset AF/AFL of < 48 hours in the ED.94-99
Spontaneous conversion within the first 48 hours
of the initial onset of AF may occur in nearly 50% of
patients, and one strategy advocated by the Canadian Cardiovascular Society for patients presenting immediately after onset of symptoms is to rate
control the patient while awaiting spontaneous
cardioversion. In this strategy, select patients may be
started on a rate control agent and instructed to return the following day for reevaluation and possible
cardioversion if they do not spontaneously return to
sinus rhythm.
Table 3. Factors Associated With Failed
Cardioversion21
•
•
•
•
•
•
Underlying illness (eg, congestive heart failure, thyrotoxicosis,
valvular disease)
Dilated left atrium
Longer duration of atrial fibrillation
Too-low energy
Technique
Other patient factors
Table 4. Strategies To Improve Direct
Current Cardioversion In The Unstable
Patient
•
•
•
360 J monophasic or 200 J biphasic synchronized shock
Time shock delivery during patient’s full expiration for optimal
energy delivery
Apex-anterior, apex-posterior, and anterior-posterior pad placement are all effective, although anterior-posterior may be more
useful with biphasic defibrillators
February 2013 • www.ebmedicine.net
7
Emergency Medicine Practice © 2013
Recent studies of elective ED cardioversion
(EDCV) have suggested a high rate of success with
few complications in low-risk patients. In numerous studies, EDCV has been shown to be safe and to
decrease hospital length of stay. A few studies have
shown it may allow for safe discharge of select patients from the ED.93-95,100-109 Choosing appropriate
patients for EDCV is of some concern, as multiple
studies have shown that patients may not be able to
correctly identify the time of onset of AF based on
their symptoms.23,36,44
Some controversy exists regarding rate control
prior to EDCV. Only 2 large studies have examined
this. Blecher et al found that administering a rate control agent prior to electrical cardioversion decreased
success, with an odds ratio (OR) of 0.39 (95% confidence interval [CI], 0.21-0.74). There was no difference
in successful chemical cardioversion.110 Scheuermeyer
et al found no difference in success rates of cardioversion after initial rate control.111 Neither study found
an increase in adverse events among patients treated
with rate control prior to cardioversion.
Selecting A Rate Control Agent
In rapid AF/AFL, conduction of disorganized
atrial contractions occurs through the atrioventricular node, and most rate control strategies
use medications that prolong the atrioventricular
refractory periods, thus slowing atrioventricular
nodal conduction.112 (See Table 5.) In the absence
Table 5. Intravenously Administered Pharmacological Agents For Rate Control Of Atrial
Fibrillation Without An Accessory Pathway8
Drug
Class of Recommendation / Level
of Evidence
Initial Loading
Dosage
Maintenance
Dosage
Onset
Time
Potential Adverse Effects / Comments
Esmolol
Class I, LOE C
0.5 mg/kg over
1 min
0.06-0.2 mg/
kg/min*
< 5 min
Metoprolol
Class I, LOE C
2.5- to 5-mg bolus
over 2 min, up to
3 doses
NA
5 min
• Bradycardia, peripheral vascular insufficiency, hypotension, heart failure, atrioventricular block, dyspnea,
bronchospasm
• Avoid in patients with obstructive pulmonary disease
• Propranolol useful in thyrotoxicosis
Propranolol
Class I, LOE C
0.15 mg/kg
NA
5 min
Beta Blockers
Nondihydropyridine Calcium Channel Blockers
Diltiazem
Class I, LOE B
0.25 mg/kg/dose
over 2 min; may
give a second
dose at 0.35 mg/
kg/dose
5-15 mg/kg
for < 24 h
2-7 min
• Hypotension, heart failure, compromised ventricular
function
• First-line medication for patients with obstructive pulmonary disease
• Verapamil has more potent negative inotropic and vasodilator effects than diltiazem. May also increase digoxin
concentration if used in combination
Verapamil
Class I, LOE B
0.075-0.15 mg/kg
over 2 min
NA
3-5 min
0.25 mg IV every 2
h, up to 1.5 mg
0.125-0.375
mg daily IV
or orally
30-180 min
• Digitalis toxicity, heart block
• Most useful in combination with a beta blocker or
calcium channel blocker for patients with congestive
heart failure
150 mg over 10
min
0.5 to 1 mg/
min IV
< 20 min
• Hypotension, prolonged QT, bradyarrhythmias
• Useful as a second-line agent or in patients with congestive heart failure
2 g over 15 min
NA
< 5 min
• Hypotension, respiratory muscle fatigue, cardiac pauses
at high doses
• Can accumulate rapidly in patients with renal failure
Cardiac Glycoside
Digoxin
Class I, LOE B
Class III Antiarrhythmic Agent
Amiodarone
Class IIa, LOE C
Adjunctive Therapies
Magnesium
NA
*Very short half-life; needs careful monitoring and titration of dose.
Abbreviations: IV, intravenous; LOE, level of evidence; NA, not applicable.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibril executive summary: a report of
the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(16):1979-2030. By permission of the
European Society of Cardiology.
Emergency Medicine Practice © 20138
www.ebmedicine.net • February 2013
of preexcitation syndromes, beta blockers and
nondihydropyridine calcium channel blockers
such as diltiazem and verapamil are effective
atrioventricular nodal blocking agents and can
safely achieve rate control in most patients.113-121
These agents work quickly, by slowing the atrioventricular conduction and prolonging refractoriness in the atrioventricular node, thus slowing
the ventricular response to AF/AFL.122 Digoxin
is a weak atrioventricular nodal blocking agent,
achieves rate control via its vagal tonic effect, and
is more effective when the patient is at rest or in
combination with another atrioventricular nodal
blocking agent.
Circumstances may exist where selection of
specific rate or rhythm strategies may benefit special
populations such as pregnant women and those
with underlying pulmonary disease, congestive
heart failure, acute myocardial infarction, and hyperthyroidism. (See Table 6, pages 9 and 10.)
Beta Blockers
In the absence of preexcitation syndromes, beta
blockers should be the first drug of choice in patients with congestive heart failure or left ventricular
dysfunction, hypertension, and acute coronary syndromes. Beta blockers may be beneficial for postoperative patients who may have new-onset AF/AFL
secondary to adrenergic surge.123,124 Propranolol
may be especially beneficial in patients with underlying hyperthyroidism or thyrotoxicosis. Beta blockers should be used with caution in patients with
hypotension or acutely decompensated heart failure.
Nondihydropyridine Calcium Channel Blockers
Nondihydropyridine calcium channel blockers (such
Table 6. Evidence-Based Recommendations: Special Circumstances For Pharmacological And
Electrical Rate And Rhythm Control Strategies For Atrial Fibrillation8 (Continued on page 10)
Class of Evidence
Recommendation
Indication (Level of Evidence)
Acute Myocardial Infarction
Class I Recommendations
DCC
Severe hemodynamic compromise, intractable ischemia, adequate rate control cannot
be achieved with pharmacological agents (Level of Evidence C)
IV beta blockers, IV nondihydropyridine calcium channel antagonists
To slow rapid ventricular response in patients who do not display chronic LV dysfunction, bronchospasm, or AV block (Level of Evidence C)
IV amiodarone
To slow rapid ventricular response and improve LV function (Level of Evidence C)
Class IIa Recommendations
IV digoxin
Patients with severe LV dysfunction and heart failure (Level of Evidence C)
Class III Recommendations
Propafenone, flecainide
Contraindicated (Level of Evidence C)
Wolff-Parkinson-White Preexcitation Syndrome
Class I Recommendations
DCC
Prevent ventricular fibrillation in patients with short anterograde bypass tract refractory period if AF occurs with rapid ventricular response associated with hemodynamic
instability (Level of Evidence B)
IV procainamide, IV ibutilide
Rapid AF without hemodynamic instability in association with wide QRS ≥ 120 ms or
rapid preexcited ventricular response (Level of Evidence C)
Class IIa Recommendations
DCC
IV flecainide
Rapid ventricular rates involving conduction over an accessory pathway (Level of
Evidence B)
Class IIb Recommendations
IV quinidine, procainamide, ibutilide,
or amiodarone
Hemodynamically stable patients with AF involving conduction over an accessory pathway (Level of Evidence B)
Class III Recommendations
IV digitalis glycosides, beta blockers,
or nondihydropyridine calcium
channel antagonists
Contraindicated (Level of Evidence C)
Beta blocker
Control ventricular response rate in patients with AF complicating thyrotoxicosis, unless
contraindicated (Level of Evidence B)
Calcium channel blocker
If beta blocker cannot be used (Level of Evidence B)
Oral anticoagulation
Prevent thromboembolism as recommended for AF patients with other stroke risk factors (Level of Evidence C). Once euthyroid state is restored, recommendations for
antithrombotic prophylaxis are the same as for patients without hyperthyroidism (Level
of Evidence C)
Hyperthyroidism
Class I Recommendations
Abbreviations: AF, atrial fibrillation; AV, atrioventricular; DCC, direct current cardioversion; IV, intravenous; LV, left ventricular.
February 2013 • www.ebmedicine.net
9
Emergency Medicine Practice © 2013
as diltiazem and verapamil) are another first-line
medication for the treatment of acute AF. They can
be useful when there are contraindications to the
use of beta blockers for patients with obstructive
pulmonary disease or can be used as a second-line
choice for thyrotoxicosis when beta blockers cannot
be used.
Diltiazem tends to be more popular than verapamil for acute rate control, as verapamil has more
potent negative inotropic and vasodilator effects
that may lead to hypotension.120 Aside from esmolol, diltiazem has a faster time of onset than beta
blockers115,124 and has been shown in a randomized
controlled trial to be more effective in controlling the
ventricular rate than IV amiodarone or digoxin.125
Digoxin
Digoxin was once the medication of choice for AF,
but it has largely been replaced by more potent
atrioventricular nodal blockers.126 Digoxin has both
negative chronotropic and positive inotropic effects,
which is particularly useful in patients with congestive heart failure, but the onset of action may take up
to 3 hours, and the full effect of digoxin may not be
felt for up to 6 hours. It can also be especially useful
in hypotensive patients due to its lack of effect on
systemic blood pressure.127,128
When used in combination with beta blockers and calcium channel blockers, digoxin has a
synergistic effect, with improved rate control and
expanded use for patients with congestive heart fail-
Table 6. Evidence-Based Recommendations: Special Circumstances For Pharmacological And
Electrical Rate And Rhythm Control Strategies For Atrial Fibrillation8 (Continued from page 9)
Class of Evidence
Recommendation
Indication (Level of Evidence)
DCC
Can be performed safely at all stages of pregnancy and is recommended in patients
who are hemodynamically unstable and whenever the risk of ongoing AF is considered high for the mother or for the fetus (Level of Evidence C)
Anticoagulation
Administration of an oral vitamin K antagonist is recommended from the second trimester until 1 month before expected delivery (Level of Evidence B)
Subcutaneous administration of LMWH in weight-adjusted therapeutic doses is recommended during the first trimester and the last month of pregnancy. Alternatively, UFH
may be given to prolong the activated PTT to 1.5 times the control (Level of Evidence
B)
Class IIa Recommendations
Beta blocker, nondihydropyridine
calcium channel antagonist
If rate control is necessary, a beta blocker or nondihydropyridine calcium channel
antagonist should be considered. During the first trimester of pregnancy, the use of a
beta blocker must be weighed against the potential risk of negative fetal effects (Level
of Evidence C)
Class IIb Recommendations
Digoxin
If rate control is necessary and a beta blocker or nondihydropyridine calcium channel
antagonist is contraindicated, digoxin may be considered (Level of Evidence C)
IV flecainide, IV ibutilide
In hemodynamically stable patients with structurally normal hearts, flecainide or ibutilide
may be considered to terminate recent-onset AF if conversion is mandatory and DCC
is inappropriate (Level of Evidence C)
Correct hypoxemia and acidosis
Primary therapeutic measure for acute pulmonary illness or exacerbation of chronic
pulmonary disease (Level of Evidence C)
Nondihydropyridine calcium channel
antagonist
To control the ventricular rate in patients with obstructive pulmonary disease (Level of
Evidence C)
DCC
Attempt in patients with pulmonary disease who become hemodynamically unstable
(Level of Evidence C)
Theophylline and beta-adrenergic
agonists
Contraindicated in patients with bronchospastic lung disease with AF (Level of Evidence C)
Beta blocker, sotalol, propafenone,
and adenosine
Contraindicated in patients with obstructive lung disease with AF (Level of Evidence C)
Pregnancy
Class I Recommendations
Pulmonary Disease
Class I Recommendations
Class III Recommendations
Abbreviations: AF, atrial fibrillation; AV, atrioventricular; DCC, direct current cardioversion; IV, intravenous; LMWH, low-molecular-weight heparin; LV, left
ventricular; PTT, partial thromboplastin time; UFH, unfractionated heparin.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibril executive summary: a report of
the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(16):1979-2030. By permission of the
European Society of Cardiology.
Emergency Medicine Practice © 201310
www.ebmedicine.net • February 2013
ure.129-131 The combination of atenolol and digoxin
may have the best rate controlling effect; however,
this combination can precipitate severe bradycardia
and should be used with caution.125 Verapamil may
increase the concentration of digoxin despite its
synergist effects.132
Table 7. Details Of The Ottawa Aggressive
Protocol For Emergency Department
Patients With Recent-Onset Atrial
Fibrillation94
1. Assessment
• Stable without ischemia, hypotension, or acute CHF?
• Onset clear and < 48 h?
• Severity of symptoms?
• Previous episodes and treatments?
• Anticoagulated with warfarin and INR therapeutic?
Amiodarone
Amiodarone, an antiarrhythmic drug, is widely used
as a rate-controlling agent, and IV administration
can lower the ventricular response in patients with
acute-onset AF through atrioventricular nodal blockade via indirect sympatholytic action.91,133,134 It is a
second-line agent due to its slower onset and greater
potential for adverse side effects.125,135 Amiodarone
has fewer negative inotropic effects, and it may be a
useful alternative agent for those who cannot tolerate
beta blockers or calcium channel blockers (such as patients with decompensated congestive heart failure).77
Amiodarone is a Class III antiarrhythmic agent, and
it should be used with caution in those who are not
anticoagulated or in those who are at high risk for
thrombotic events, as it can promote cardioversion.
2. Rate control
• If highly symptomatic or not planning to convert
• Diltiazem IV (0.25 mg/kg over 10 min; repeat at 0.35 mg/kg)
• Metoprolol IV (5-mg doses q15min)
3. Pharmacologic cardioversion
• Procainamide IV (1 g IV over 60 min; hold if SBP < 100 mg Hg)
4. Electrical cardioversion
• Consider keeping patient NPO x 6 h
• Procedural sedation and analgesia given by emergency physician (propofol IV and fentanyl IV)
• Start at 150-200 J biphasic synchronized*
• Use anterior-posterior pads, especially if not responding
Magnesium
Magnesium decreases conduction through the atrioventricular node, and it has been shown in multiple
small studies to have some effect in decreasing the
ventricular response to AF;136-141 however, its use is
most often recommended as an adjunctive therapy.
Magnesium has few negative inotropic effects and is
generally well tolerated with few side effects other
than flushing, warmth, and tingling. Rapid infusion
and large doses may be associated with respiratory
muscle fatigue, hypotension, and cardiac pauses.136
Magnesium may also promote conversion to sinus
rhythm, with some studies showing 50% to 60% of
patients converted to sinus rhythm.136,137,139
5. Anticoagulation
• Usually no heparin or warfarin for most patients if onset clearly <
48 h or if therapeutic INR for > 3 wk
6. Disposition
• Home within 1 h after cardioversion
• Usually no antiarrhythmic prophylaxis or anticoagulation given
• Arrange outpatient echocardiography if first episode
• Cardiology follow-up if first episode or frequent episodes
7. Patients not treated with cardioversion
• Achieve rate control with diltiazem IV (target heart rate < 100
bpm)
• Discharge home on diltiazem (or metoprolol)
• Discharge home on warfarin and arrange INR monitoring
• Arrange outpatient echocardiography
• Follow up with cardiology at 4 wk for elective cardioversion
Rhythm Control Strategies: Electrical And
Pharmacological Cardioversion
The development of new drugs for pharmacological
conversion has increased its popularity; however,
DCC with biphasic shocks remains more effective.
Elective DCC is painful, and it requires procedural
sedation or anesthesia. The Ottawa Aggressive
Protocol is a rapid ED strategy that has been in use
in Canadian EDs for several years. (See Table 7.) A
prospective review of 660 patient visits using this
protocol found successful conversion of 85% of patients with new-onset AF as well as a decreased ED
length of stay, few side effects, and low ED recidivism rates with repeat episodes of AF.94 Additional
studies have shown a shorter ED length of stay
among patients who are electrically cardioverted
compared to those treated with oral or IV antiarrhythmic medications.106,107
February 2013 • www.ebmedicine.net
8. Recommend additions to protocol
• Consider TEE if onset unclear
• Alternate rhythm-control drugs: propafenone, amiodarone
• If TEE-guided cardioversion > 48 h, start warfarin
• If CHADS score ≥ 1, consider warfarin and arrange early follow-up
*Most patients treated with electrical cardioversion in the current study
were managed with monophasic cardioversion.
Abbreviations: bpm, beats per minute; CHF, congestive heart failure;
INR, international normalized ratio; IV, intravenous; NPO, nil per os
(nothing by mouth); SBP, systolic blood pressure; TEE, transesophageal echocardiography.
Stiell IG, Clement CM, Perry JJ, et al. Association of the Ottawa
Aggressive Protocol with rapid discharge of emergency department patients with recent-onset atrial fibrillation or flutter. CJEM.
2010;12(3):181-191. Reprinted with permission of Decker Publishing, Inc.
11
Emergency Medicine Practice © 2013
proarrhythmia risk factors should be conducted.
Patients who receive pharmacologic cardioversion
should have normal electrolytes and a normal QTc
interval. Depressed left ventricular function or underlying structural heart disease may preclude some
patients from certain agents. (See Tables 8 and 9.)
Since the release of the 2006 ACC/AHA/ECS
guidelines, procainamide has been studied for use in
cardioversion of new-onset AF/AFL patients in the
ED, with successful conversion in 52% to 58% of cases and a low rate of adverse events and no deaths.
In a Canadian series, the most common side effect
of procainamide administration was temporary
hypotension (6.7%-8.5%), and most patients were
discharged home from the ED with no episodes of
torsades de pointes, stroke, or death.94,107
Pharmacological Enhancement Of Direct Current
Cardioversion
Pretreatment with an antiarrhythmic agent such as
amiodarone, flecainide, ibutilide, propafenone, or
sotalol may increase the success of DCC and should
be considered in patients for whom electrical cardioversion initially fails (Class IIa, LOE C). Alternatively, failure of an antiarrhythmic agent followed by
an observation period may be followed with electrical cardioversion in the ED, as demonstrated by the
Ottawa Aggressive Protocol.
Selecting Agents for Pharmacological Cardioversion
Of AF/AFL
Prior to selecting a pharmacological agent to cardiovert a patient with AF, an assessment of the patient’s
Table 8. Intravenously And Orally Administered Pharmacological Agents For Cardioversion Of
Atrial Fibrillation8
Class of Recommendation / Level of Evidence
Route of Administration
Initial Loading Dosage
Class IIa,
LOE B
Oral
200-300 mg
IV
1.5-3.5 mg/kg over 10-20
min
Drug
AF of up to
7-day duration
AF present for
> 7 days
AF with Preexcitation
Flecainide
Class Ia, LOE A
Class IIb, LOE B
Potential Adverse
Effects
Hypotension, atrial
flutter with high ventricular rate
Ibutilide
Class Ia, LOE A
Class IIa, LOE A
Class I,
LOE C
IV
1 mg over 10 min; repeat 1
mg when necessary
QT prolongation, torsades de pointes
Propafenone
Class Ia, LOE A
Class IIb, LOE B
NA
Oral
600 mg
IV
1.5-2.0 mg/kg over 10-20
min
Hypotension, atrial
flutter with high ventricular rate
Oral
Creatinine
clearance
(mL/min)
> 60
40-60
20-40
Dofetilide
Amiodarone
Class Ia, LOE A
Class IIa, LOE A
Class Ia, LOE A
Class IIa, LOE A
NA
Class IIb,
LOE B
Dosage
(mcg bid)
500
250
125
Oral
1.2-1.8 g/d in divided
doses until 10 g total
IV
5-7 mg/kg over 30-60 min,
then 1.2-1.8 g/day continuous IV or divided oral
doses until 10 g total
QT prolongation,
torsades de pointes;
adjust dose for renal
function, body size,
and age
Hypotension, bradycardia, QT prolongation,
torsades de pointes,
GI upset, constipation,
phlebitis (IV)
Procainamide
Class IIb, LOE B
Class IIb, LOE C
Class I,
LOE C
IV
1 g IV over 60 min
Hypotension, QT prolongation, torsades de
pointes
Quinidine
Class IIb, LOE B
Class IIb, LOE B
Class IIb,
LOE B
Oral
0.75-1.5 g in divided doses
over 6-12 h, usually with
a rate-slowing drug
QT prolongation, torsades de pointes, GI
upset, hypotension
Abbreviations: AF, atrial fibrillation; bid, two times per day; GI, gastrointestinal; IV, intravenous; LOE, level of evidence; NA, not applicable.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation-executive summary: a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(16):1979-2030. By permission of the
European Society of Cardiology.
Emergency Medicine Practice © 201312
www.ebmedicine.net • February 2013
Preexcitation syndromes such as Wolff-Parkinson-White syndrome may be particularly challenging
to manage in patients with AF, as the short refractory period of the accessory pathway can result in
extremely fast ventricular rates, and use of atrioventricular nodal blocking agents such as beta blockers,
calcium channel blockers, and digoxin may induce
ventricular fibrillation and are contraindicated.
Synchronized electrical cardioversion is the
primary treatment for unstable patients with an accessory pathway or those who present with a very
rapid heart rate, even if stable. Class Ia drugs such as
procainamide and quinidine, or class Ic drugs such
as flecainide, slow conduction through the accessory
pathway and prolong the refractory period in the
bypass tract, and they can be safely used in patients
in rapid AF with Wolff-Parkinson-White syndrome.
Amiodarone may also be used, although it has
not been shown to be safer or more effective than
procainamide among patients with Wolff-ParkinsonWhite preexcitation syndrome.142
Thromboembolic events in all patients who
are cardioverted appear to be as high as 5% to
7% without anticoagulation but can decrease to <
1.6% if cardioversion occurs after 2 to 4 weeks of
anticoagulation or shorter-term anticoagulation
and a negative screening transesophageal echocardiogram.64,69,144 The rate of embolic events among
patients with spontaneous or active cardioversion
within the first 48 hours of AF onset appears to be
very similar to the reported incidence of embolism
after anticoagulation for 3 to 4 weeks.144 Some studies, however, have shown that patients may not be
able to correctly identify the time of onset of AF
based on their symptoms,23,36,44 and the use of transesophageal echocardiography has shown that a clot
may be present in the atrium up to 13% of the time
in patients with AF < 72 hours duration; thus, it is
recommended that patients be anticoagulated prior
to cardioversion and anticoagulated for 3 to 4 weeks
after cardioversion unless they are low risk or it is
contraindicated.
The following recommendations are excerpted
with permission by the European Society of Cardiology from: “ACC/AHA/ESC 2006 Guidelines for
the Management of Patients with Atrial FibrillationExecutive Summary: a Report of the American
College Of Cardiology/American Heart Association
Task Force On Practice Guidelines and the European Society Of Cardiology Committee for Practice
Guidelines (Writing Committee to Revise the 2001
Guidelines for the Management of Patients with
Atrial Fibrillation) developed in collaboration with
the European Heart Rhythm Association and the
Heart Rhythm Society:”
“Class I Recommendations For Immediate
Cardioversion: For patients with AF of more than 48
hours duration requiring immediate cardioversion
Reducing Stroke Risk
Prevention Of Postconversion Thromboembolism
AF and AFL are associated with an increased longterm risk of stroke and an increased risk of thromboembolism in the postconversion period.42 Stagnant
blood flow in the dysfunctional atria can lead to clot
formation in the atria or atrial appendage, which can
subsequently lead to embolization and cerebral vascular occlusion prior to or after cardioversion.42,146
Cardioversion to sinus rhythm may result in atrial
“stunning,” which is further mechanical dysfunction of the atria that may last up to several weeks,
further increasing the risk of thromboembolism even
in patients with a negative transesophageal echocardiography prior to cardioversion.143
Table 9. Intravenously Administered Pharmacological Agents For Rate And Rhythm Control Of
Atrial Fibrillation With An Accessory Pathway8
Drug
Class of Recommendation /
Level of Evidence
Initial Loading Dosage
Potential Adverse Effects
Procainamide
Class I, LOE C
1 g IV over 60 min
Hypotension, QT prolongation,
torsades de pointes
Ibutilide
Class I, LOE C
1 mg over 10 min; repeat 1 mg
when necessary
QT prolongation, torsades de
pointes
Flecainide
Class IIa, LOE B
1.5-3.5 mg/kg over 10-20 min
Hypotension, atrial flutter with high
ventricular rate
Amiodarone
Class IIa, LOE C
150 mg over 10 min
Hypotension, QT prolongation,
bradyarrhythmias
Abbreviation: LOE, level of evidence.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation-executive summary: a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(16):1979-2030. By permission of the
European Society of Cardiology.
February 2013 • www.ebmedicine.net
13
Emergency Medicine Practice © 2013
because of hemodynamic instability, heparin should
be administered concurrently (unless contraindicated) by an initial IV bolus injection followed by a
continuous infusion in a dose adjusted to prolong
the activated partial thromboplastin time to 1.5 to
2 times the reference control value. Thereafter, oral
anticoagulation (INR 2.0-3.0) should be provided for
at least 4 weeks, as for patients undergoing electrical
cardioversion. Limited data support subcutaneous
administration of low-molecular-weight heparin in
this indication (Level of Evidence C).”
“For patients with AF of 48 hours duration or
longer, or when the duration of AF is unknown,
anticoagulation (INR 2.0-3.0) is recommended for at
least 3 weeks prior to and 4 weeks after cardioversion, regardless of the method (electrical or pharmacological) used to restores sinus rhythm (Level
of Evidence B).”
“Class IIa Recommendations: As an alternative
to anticoagulation prior to cardioversion of AF, it is
reasonable to perform transesophageal echocardiography in search of thrombus in the left atrium or left
atrial appendage (Level of Evidence B). For patients
with no identifiable thrombus, cardioversion is
reasonable immediately after anticoagulation with
unfractionated heparin (initial IV bolus injection
followed by a continuous infusion in a dose adjusted
to prolong the activated partial thromboplastin time
to 1.5 to 2 times the reference control value until
oral anticoagulation has been established) (Level of
Evidence B). Limited data support subcutaneous
administration of low-molecular-weight heparin in
this indication (Level of Evidence C). For patients
in whom thrombus is identified by transesophageal
echocardiography, oral anticoagulation (INR 2.03.0) is reasonable for at least 3 weeks prior to and 4
weeks after restoration of sinus rhythm and a long
period of anticoagulation may be appropriate even
after apparently successful cardioversion because
the risk of thromboembolism often remains elevated
in such cases (Level of Evidence C).”
Decreasing Thromboembolic Risk
Multiple studies have been conducted to further
risk stratify patients with AF/AFL to detect who
may benefit from anticoagulation therapy to decrease stroke, transient ischemic attack, and systemic
thromboembolism. Patients at low risk (defined as
< 2% stroke risk per 100 patient-years with aspirin
as antithrombotic therapy) gain little benefit with
oral anticoagulation with vitamin K antagonists
(warfarin), and the risk of bleeding from vitamin K
antagonists outweighs the potential benefit of stroke
reduction.145 For patients at high risk (> 4% stroke
risk per 100 patient-years), vitamin K antagonists
have consistently been shown to improve qualityadjusted survival over aspirin with an acceptable
bleed rate.145,146 Vitamin K antagonists decrease
stroke risk by 66%, whereas antiplatelet therapy
Emergency Medicine Practice © 201314
with aspirin 81 mg to 325 mg decreases stroke risk
by only 22%.147
For those who cannot take vitamin K antagonists, adding clopidogrel to aspirin as an alternative to vitamin K antagonists provides some additional stroke risk reduction compared to aspirin
alone (6.8% vs 7.6%/y); however, there is a higher
rate of major bleeding in patients receiving combination therapy compared to those with aspirin
alone (2.0% vs 1.3%/y).148 This combination therapy is not as effective to reduce vascular events as
vitamin K antagonist use (5.60% vs 3.93% annual
risk);149 however, there is an increased risk of
intracranial hemorrhage among warfarin users
(0.4%).150
The Novel Oral Anticoagulants
Prior to the United States Food and Drug Administration (FDA) approval of the direct thrombin inhibitor (DTI) dabigatran (Pradaxa®) in 2010, vitamin K
antagonists were the only available oral anticoagulant options. Since then, rivaroxaban (Xarelto®), a
factor Xa inhibitor, received FDA approval in 2011,
apixaban (Eliquis®) received approval in 2012, and
edoxaban (Lixiana®) is currently undergoing phase
III clinical trials. Dabigatran, rivaroxaban, and apixaban have been shown to be noninferior to warfarin
with regards to stroke and systemic embolism, with
favorable results in safety outcomes (including major bleeding).151-156
Dabigatran was reviewed in the 2011 ACC/
AHA/ESC update, receiving a Class I, Level of
Evidence B recommendation as a useful alternative to warfarin to prevent thromboembolic events.
Subgroup analysis of the RE-LY (Randomized
Evaluation of Long-term anticoagulant therapY)
trial examining patients who were cardioverted
showed that, at 30 days, dabigatran was noninferior
to warfarin in preventing thromboembolic events in
patients anticoagulated with dabigatran prior to cardioversion.157 Decision analysis models suggest that
dabigatran may be a cost-effective strategy to reduce
thromboembolic events for people with AF at a high
risk of stroke or hemorrhage unless INR control with
warfarin was excellent.158
Stroke Risk Stratification For Preventing
Thromboembolism
In 2001, the CHADS2 (Congestive heart failure,
Hypertension, Age, Diabetes mellitus, prior Stroke,
transient ischemic attack, or thromboembolism) score
was derived by expert consensus to simplify the determination of stroke risk by combining high-risk patient factors that had been previously identified into a
simple scoring mechanism to predict thromboembolic
risk and need for anticoagulation therapy.159
The revised CHADS2 defines low risk as a score
of 0, moderate risk as a score of 1, and high risk as
a score ≥ 2. Multiple validation studies have been
www.ebmedicine.net • February 2013
published for CHADS2; however; the high level of
heterogeneity among groups in the limited studies
included led the authors to conclude that the results should be used cautiously, and further studies should be performed to guide antithrombotic
therapy. One such risk-factor-based approach includes the CHADS2-VASc risk stratification scheme.
This scoring system was created by refining the 2006
Birmingham/NICE160 criteria and adding some of
the less well-validated risk factors into a scoring
system.161 (See Table 10.) Multiple studies have validated the CHADS2VASc scoring system, finding that use of this scoring
system significantly improved the predictive value
of the CHADS2 scoring system and improved classification of patients at very low, low, and intermediate risk of stroke.163-166 The CHADS2-VASc scoring
system has been incorporated into the ESC and
Canadian Cardiovascular Society guidelines, but it
has not been adopted into the ACC/AHA guidelines for stroke prevention. (See Table 11.) The ESC
guidelines suggest using CHADS2 as an initial risk
Table 10. CHADS2/CHADS2-VASc Scoring162
Risk Factor
Score
Congestive heart failure/left ventricular dysfunction
1
Hypertension
1
Age > 75 years
2
Diabetes mellitus
1
Stroke/transient ischemic attack/thromboembolism
2
Vascular disease (prior myocardial infarction, peripheral artery disease, or aortic plaque)
1
Age 65-74 years
1
Sex category (female gender)
1
Low risk, 0; moderate risk, 1; high risk, ≥ 2.
Reproduced with permission from the American College of Chest
Physicians. Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical
risk stratification for predicting stroke and thromboembolism in atrial
fibrillation using a novel risk factor-based approach: the Euro heart
survey on atrial fibrillation. Chest. 2010;137(2):263-272.
Table 11. Evidence-Based Recommendations: ACC/AHA/ESC Risk Stratification
Recommendations For Preventing Thromboembolism8
Class of Evidence
Recommendation
Class I
No anticoagulation
Vitamin K antagonist*
Class IIa
Indication
Lone AF or contraindications to anticoagulation (LOE A)
†
Aspirin or vitamin K antagonist*†
•
•
•
•
Rheumatic mitral stenosis (LOE A)
Prior thromboembolism (stroke, TIA, or systemic embolism) (LOE A)
2 or more moderate risk factors (LOE A):
n
Congestive heart failure or ejection fraction < 35%
n
Hypertension
n
Age ≥ 75 years
n
Diabetes
AF with mechanical valves; target of intensity should be based on type of prosthesis, maintaining an INR of at least 2.5 (LOE B)
• Nonvalvular AF with 1 moderate risk factor (LOE A):
n Hypertension
n Age ≥ 75 years
n Diabetes
n Heart failure or impaired left ventricular function
• Nonvalvular AF with 1 or more less well-validated risk factor (LOE B):
n Age 65-74 years
n Female gender
n Coronary artery disease
*Dabigatran may be used in place of vitamin K antagonist (Class I, LOE B). Recently FDA-approved rivaroxaban may be considered in place of vitamin
K antagonist, but it was not included in the 2011 ACC/AHA/ESC update.
†
Combination therapy with clopidogrel and aspirin may be considered in patients with AF in whom oral anticoagulation with warfarin is considered
unsuitable (due to patient preference or ability to sustain anticoagulation) (Class IIa, LOE B).
Abbreviations: ACC, American College of Cardiology; AF, atrial fibrillation; AHA, American Heart Association; ESC, European Society of Cardiology;
INR, international normalized ratio; LOE, level of evidence; TIA, transient ischemic attack.
Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation-executive summary: a
report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (writing committee to revise the 2001 guidelines for the management of patients with atrial fibrillation) developed in
collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur Heart J. 2006;27(16):1979-2030. By permission of the
European Society of Cardiology.
February 2013 • www.ebmedicine.net
15
Emergency Medicine Practice © 2013
Clinical Pathway For Initial Approach To The
Hemodynamically Unstable Rapid Atrial Fibrillation Patient
Begin resuscitative efforts:
• Supplemental O2 and respiratory support as needed
• Large-bore peripheral IV access
• 20-40 mL/kg crystalloid fluid bolus challenge
• Treat underlying condition, further stabilize
• Consider anticoagulation
• Begin evaluation
• Anticipate decompensation
• Admit
(Class I)
Immediate DCC (Class I)
• 200 J biphasic (Class II)
• 200-360 J monophasic
(Class I)
• Can consider lower
energy for atrial flutter
(Class II)
• Anticipate failure
Further stabilize
• Consider anticoagulation
• Begin evaluation
• Anticipate decompensation
• Admit
(Class I)
YES
Other causes for hemodynamic instability present?
• Evidence of sepsis, bleeding, cardiogenic shock: treat
• underlying condition
• Bedside ultrasonography to evaluate for intravascular volume,
LV function, obstructive shock, and occult bleeding (Class I-II)
Abbreviations: AF, atrial fibrillation;
bpm, beats per minute; DCC, direct
current cardioversion; ECG, electrocardiogram; IV, intravenous; J,
joules; LV, left ventricular.
For class of evidence definitions, see
Table 1, page 2.
*Use amiodarone with caution in
these cases, as severe hypotension
has been reported.
NO
YES
• Hemodynamically unstable from AF?
or
• AF involving preexcitation with very rapid tachycardia?
• Candidate for immediate DCC?
NO
Suspicion for accessory
pathway?
• Wide, bizarre QRS
complexes
• Ventricular rate > 250
bpm
• History of Wolff-Parkinson-White sydrome
• Prior ECG with delta
wave
NO
YES
YES
Success?
NO
Repeat DCC
• Increase energy level (Class II)
• Consider anterior-posterior pad
placement for biphasic defibrillators (Class Indeterminate)
• Time with patient’s respiratory
cycle, shock during full expiration (Class Indeterminate)
YES
Success?
• Ibutilide 1 mg over 10 min followed by cardioversion (Class II-III)
or
• Rate control agents:
n Diltiazem < 0.2 mg/kg slow IV bolus or 2.5 mg/min drip up to
50 mg total
n Amiodarone (Class II-III)
n Magnesium (Class II-III)
or
• Procainamide (Class II)
or
• Further electrical cardioversion
Consider:
• Vasopressors (Class Indeterminate)
• Calcium gluconate (Class Indeterminate)
• Amiodarone* (Class II-III)
or
• Procainamide (Class II)
or
• Ibutilide 1 mg IV over 1 min
(Class II-III)
Consider:
• Vasopressors
• Calcium gluconate
• Electrical cardioversion
(Class Indeterminate)
NO
NO
Emergency Medicine Practice © 201316
• Diltiazem < 0.2 mg/kg slow IV
bolus or 2.5 mg/min drip up to 50
mg total
or
• Amiodarone* (Class II-III)
or
• Magnesium (Class II-III)
Consider:
• Vasopressors
• Calcium gluconate
• Electrical cardioversion
Suspicion for accessory pathway?
• Wide, bizarre QRS complexes
• Ventricular rate > 250 bpm
• History of Wolff-Parkinson-White syndrome?
• Prior ECG with delta wave
YES
• Procainamide (Class II)
or
• Ibutilide 1 mg IV over 1+ min (Class II-III)
or
• Amiodarone* (Class II-III)
or
• Further electrical cardioversion
Consider:
• Vasopressors (Class Indeterminate)
• Calcium gluconate (Class Indeterminate)
www.ebmedicine.net • February 2013
Clinical Pathway For Rate Control For Stable Patients With New-Onset
Atrial Fibrillation With Rapid Ventricular Response
Suspicion for accessory pathway?
• Wide, bizarre QRS complexes (> 120 ms)
• History of Wolff-Parkinson-White syndrome
• Delta wave on ECG
• Very rapid ventricular rate > 250 bpm
YES
NO
• Consider need for anticoagulation
• Contraindications to sedation of
DCC?
YES
• Procainamide
(Class II)
or
• Amiodarone
(Class III)
NO
Suspicion for myocardial infarction,
left ventricular dysfunction,
or thyrotoxicosis?
YES
• Electrical
cardioversion (Class
I-II)
or
• Procainamide
(Class II)
or
• Amiodarone
(Class III)
Contraindication to
calcium channel blockers?
YES
Contraindications to beta blocker?
YES
• Avoid beta blockers (Class I)
• Consider esmolol if nonsignificant
contraindications (Class III)
• Verapamil (Class I-II) 2.5 mg IV
q10-15 min until heart rate < 120,
conversion, hypotension, or max
20 mg
or
• Diltiazem (Class I-II) 0.25 mg/kg
IV over 2 min (followed by bolus of
0.35 mg/kg IV over 2 min if inadequate response at 15 min) until
rate < 120, conversion, hypotension, or max 50 mg
or
• Amiodarone 150 mg IV over 10
min (Class II-III)
NO
NO
Beta blocker
for rate
control
(Class I-II)
Abbreviations: bpm, beats per minute; CHF, congestive heart
failure; DCC, direct current cardioversion; ECG, electrocardiogram; IV, intravenous.
For class of evidence definitions, see Table 1, page 2.
NO
Consider:
• Esmolol (Class II-III)
or
• Cardioversion (Class II): Consider
anticoagulation and sedation issues
or
• Magnesium (Class II-III)
or
• Digoxin (in addition to another
agent) (Class II)
or
• Amiodarone 150 mg IV over 10
min (Class II-III)
• Diltiazem 5 mg slow IV q5min until
heart rate < 120 bpm, conversion,
or 50-mg maximum dose
• Consider drip after bolus (Class
I-II)
or
• 2.5 mg/min continuous drip until
HR < 100 bpm or 50-mg maximum
dose (Class Indeterminate)
or
• Amiodarone 150 mg bolus, then
drip or repeat bolus (Class Indeterminate)
Consider adjunct treatment:
• Magnesium (Class II)
or
• Digoxin (Class II)
Avoid beta blockers (Class I-II)
Emergency Medicine Practice © 201317
CHF or borderline blood pressure?
YES
Pretreat with
5-10 cc calcium gluconate
slow IV push
(Class I-II)
NO
Consider
pretreatment
with calcium
(Class II)
• Verapamil (Class I-II) 2.5 mg IV
q10-15 min until heart rate < 120
bpm, conversion, hypotension, or
20-mg maximum dose
or
• Diltiazem (Class I-II) 0.25 mg/kg
IV over 2 min (followed by bolus of
0.35 mg/kg IV over 2 min if inadequate response at 15 min) until
heart rate < 120 bpm, conversion,
hypotension, or 50-mg maximum
dose
Consider adjunct treatment:
• Magnesium (Class II)
or
• Digoxin (Class II)
Avoid beta blockers (Class I-II)
www.ebmedicine.net • February 2013
stratification tool to identify high-risk individuals;
those with CHADS2 scores ≥ 2 should be placed
on chronic oral anticoagulation. In patients with
a CHADS2 score of 0-1, or when a more detailed
stroke risk assessment should be conducted, the
CHADS2-VASc score is recommended in order to
include additional risk factors as part of the criteria.
Bleeding Risk In Anticoagulation Therapy
While anticoagulation has been shown to decrease
the risk of ischemic stroke, patients are more likely
to experience major bleeding. A systematic review
of physicians’ attitudes regarding anticoagulation
found that physicians were reluctant to prescribe
warfarin for elderly patients due to bleeding concerns, despite the increased benefit in these patients
compared to younger patients167-170 and some
evidence of safe use in the elderly on vitamin K
antagonists.161,171-173
To provide objective risk stratification to assess
bleeding risk, various tools have been developed (eg,
HAS-BLED). HAS-BLED was created by multivariate analysis of risk factors associated with bleeding
among patients with AF/AFL undergoing antithrombotic therapy with vitamin K antagonists174 and has
been validated by multiple studies and shown to
have better predictive value than other tools.175-179
Analyses of the HAS-BLED score have shown
that for the risk of bleeding to outweigh the benefit
of anticoagulation, the HAS-BLED score should
exceed the stroke risk calculated by CHADS2. (See
Table 12.) For example, for the majority of high-risk
patients who should be anticoagulated (CHADS2 ≥
2), the HAS-BLED score must also exceed 2 for the
potential harm of bleeding to outweigh the potential
benefit of stroke prevention.The use of HAS-BLED
is recommended by the Canadian Cardiovascular
Society and the ESC but has not been adopted into
the ACC/AHA guidelines.
Disposition
Strategies to determine which patients who present
to the ED in new-onset AF/AFL can be safely discharged home are becoming increasingly important.
Multiple studies have found the total direct cost per
patient with AF to be much higher than patients
without AF, at roughly $20,670 each year, in contrast
to the average healthcare cost of $11,965 among
patients without AF.7 Each documented recurrence
of AF increases annual healthcare costs by approximately $1600.180 The level of acute care can vary
among individuals, but the principal cost driver was
found to be inpatient service charge.181 A study done
in Canada showed the average length of hospitalization for an AF patient was roughly 5.7 days.182 The
total monetary burden is expected to increase over
the next few decades, especially since the anticiEmergency Medicine Practice © 201318
pated number of older adults with AF is expected to
double over the next 3 decades.183
Few studies of EDCV and discharge have been
performed. They are mostly retrospective, but all
have had favorable results. EDCV has a success
rate of 86% to 92%, with decreased overall hospital
length of stay, few complications, and high patient
satisfaction, with only a 3% to 17% recidivism rate
for relapsed AF.94,95,101,102,105
ED disposition is addressed only in the Canadian Cardiovascular Society guidelines, which recommend admission of new-onset AF only for patients
with decompensated heart failure or myocardial
ischemia or for patients who are highly symptomatic and in whom adequate rate control cannot
be achieved. It is recommended by the Canadian
Cardiovascular Society that other patients should be
discharged after rate or rhythm control with outpatient cardiology consultation.
It is suggested that truly low-risk patients may
be able to go home safely if they meet the following
criteria:
• < 60 years of age
• No significant comorbid disease
• No clinical suspicion for pulmonary embolism
or myocardial infarction
• Conversion in ED or rate control
Urgent cardiology follow-up is mandatory for
all patients with new-onset AF who are being discharged.
Table 12. HAS-BLED Scoring176
HAS-BLED Acronym
Score
HAS-BLED
Score*
Bleeds per 100
patient-years
Hypertension
1
1
1.13
Abnormal renal and
liver function (1
point each)
1 or 2
2
1.02
Stroke
1
3
1.88
Bleeding history or
predisposition
1
4
3.74
Labile INRs
1
Elderly (> 65 years
of age)
1
Drugs or alcohol
concomitantly (1
point each)
1 or 2
8.70
*Insufficient data for analysis of bleeds with HAS-BLED score ≥ 5.
Abbreviation: INR, international normalized ratio.
Reproduced with permission from the American College of Chest
Physicians. Pisters R, Lane DA, Nieuwlaat R, et al. A novel userfriendly score (HAS-BLED) to assess 1-year risk of major bleeding in patients with atrial fibrillation: the Euro heart survey. Chest.
2010;138(5):1093-1100.
www.ebmedicine.net • February 2013
appearing aorta. The ECG (shown below) confirmed
AF, and you placed the defibrillator pads on the patient
in an anterior-posterior position. You direct current
cardioverted him with a biphasic cardioverter using
200 J. The patient then became more awake, he was able
to converse with you, and his blood pressure rose to
125/73 mm Hg. He had a CHADS2 score of 3 and no
contraindications to anticoagulation, so you began a
heparin drip and admitted him to a monitored unit.
Summary
AF/AFL are the most common cardiac arrhythmias
encountered. As the United States population ages,
we will likely encounter more cases of AF/AFL, and
complications from these cardiac arrhythmias (such
as thromboembolic events). Emergency clinicians
must possess evidence-based knowledge of multiple approaches to rate or rhythm control in order
to manage the AF/AFL patient, whom and when to
anticoagulate, and cost-effective strategies to evaluate new-onset AF/AFL.
Case Conclusions
The first patient’s ECG (shown below) shows AF with
preexcitation consistent with Wolff-Parkinson-White syndrome. Because the patient was hemodynamically stable,
you obtained 2 large-bore peripheral IV lines and began
an infusion of procainamide, coadministering a normal
saline bolus. She converted to normal sinus rhythm and
felt much improved, with normal repeat vital signs. Her
repeat ECG showed a short PR interval with delta waves.
She had no prior history of this, no past medical history,
and a CHADS2 score of 0. You consulted cardiology for an
electrophysiology study, and she was successfully ablated
and discharged home.
Image used with permission of www.ecglibrary.com.
References
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are
equally robust. The findings of a large, prospective,
random­ized, and blinded trial should carry more
weight than a case report.
To help the reader judge the strength of each
reference, pertinent information about the study
will be included in bold type following the ref­
erence, where available. In addition, the most informative references cited in this paper, as determined
by the authors, are noted by an asterisk (*) next to
the number of the reference.
1.
Image used with permission of www.ecglibrary.com.
You thought the second patient’s hypotension
might have been due to sepsis; however, the irregular
rhythm on the monitor appeared to be rapid AF, and the
loss of atrial kick and decreased ejection fraction may
have contributed to his hypotension. While the ECG
was being performed, you “pressure-bagged” 2 500cc normal saline boluses through 18-g peripheral IVs
and obtained slightly improved hemodynamics, with
a heart rate of 140 beats/min per minute and a blood
pressure of 102/64 mm Hg but no improvement in his
mental status. You performed a bedside ultrasound that
showed a 2.5-cm inferior vena cava without respiratory variation, no pericardial effusion, a normal LV:RV
ratio, no free fluid in the abdomen, and a normalFebruary 2013 • www.ebmedicine.net
2.
3.
4.
19
Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESC
guidelines for the management of patients with atrial fibrillation: executive summary A report of the American College
of Cardiology/American Heart Association Task Force on
Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines and Policy Conferences
(Committee to Develop Guidelines for the Management of
Patients with Atrial Fibrillation) developed in collaboration
with the North American Society of Pacing and Electrophysiology. Circulation. 2001;104(17):2118-2150. (Evidence-based
review)
European Heart Rhythm Association, European Association
for Cardio-Thoracic Surgery, Camm AJ, et al. Guidelines for
the management of atrial fibrillation: the task force for the
management of atrial fibrillation of the European Society
of Cardiology (ESC). Eur Heart J. 2010;31(19):2369-2429.
(Evidence-based review)
Naccarelli GV, Varker H, Lin J, et al. Increasing prevalence of
atrial fibrillation and flutter in the United States. Am J Cardiol. 2009;104(11):1534-1539. (Retrospective database review)
Lanzarotti CJ, Olshansky B. Thromboembolism in chronic
Emergency Medicine Practice © 2013
atrial flutter: is the risk underestimated? J Am Coll Cardiol.
1997;30(6):1506-1511. (Retrospective review, 110 patients)
5. Ghali WA, Wasil BI, Brant R, et al. Atrial flutter and the risk
of thromboembolism: a systematic review and meta-analysis.
Am J Med. 2005;118(2):101-107. (Systematic review and metaanalysis; 13 observational studies)
6. Coyne KS, Paramore C, Grandy S, et al. Assessing the direct
costs of treating nonvalvular atrial fibrillation in the United
States. Value Health. 2006;9(5):348-356. (Retrospective database review)
7. Kim MH, Johnston SS, Chu BC, et al. Estimation of total
incremental health care costs in patients with atrial fibrillation in the United States. Circ Cardiovasc Qual Outcomes.
2011;4(3):313-320. (Retrospective observational cohort
study; 89,066 patients)
8.* Fuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006
guidelines for the management of patients with atrial fibrillation: executive summary: a report of the American College
of Cardiology/American Heart Association Task Force on
Practice Guidelines and the European Society of Cardiology
Committee for Practice Guidelines (writing committee to
revise the 2001 guidelines for the management of patients
with atrial fibrillation) developed in collaboration with the
European Heart Rhythm Association and the Heart Rhythm
Society. Eur Heart J. 2006;27(16):1979-2030. (Clinical guidelines)
9. Wann LS, Curtis AB, Ellenbogen KA, et al. 2011 ACCF/
AHA/HRS focused update on the management of patients
with atrial fibrillation (update on dabigatran): a report of
the American College of Cardiology Foundation/American
Heart Association Task Force on Practice Guidelines. J Am
Coll Cardiol. 2011;57(11):1330-1337. (Evidence-based review)
10. Cairns JA, Connolly S, McMurtry S, et al. Canadian Cardiovascular Society atrial fibrillation guidelines 2010: prevention of stroke and systemic thromboembolism in atrial
fibrillation and flutter. Can J Cardiol. 2011;27(1):74-90.
Risk Management Pitfalls For Atrial Fibrillation (continued on page 21)
1. “The patient denied any chest pain, so I sent
her home after she spontaneously cardioverted.” Unfortunately, the patient was a 62-year-old
female with diabetes who had a prior history of
myocardial infarction. Had you compared her
prior ECG, you would have noted new ischemic
changes. Although she spontaneously converted,
ECG changes and significant cardiac risk factors
should have prompted an admission to further
evaluate for ischemia.
2. “The ibutilide worked great. The patient felt
much better and wanted to go home immediately.”
While ibutilide works to convert AF/AFL
approximately 40% to 50% of the time, it has
significant risks—most notably an 8% risk
of torsades de pointes and other ventricular
tachyarrhythmias, which may be mitigated by
pretreatment with IV magnesium sulfate. Use of
this drug requires a 4-hour period of monitoring
after administration.
3. “The QRS complexes looked a little bizarre,
but I figured she had an underlying bundle
branch block. I didn’t think a 20-mg diltiazem
bolus would cause her to go into cardiac arrest.”
Wide, bizarre QRS complexes with very rapid
ventricular rates up to 300 beats per minute
should lead you to suspect preexcitation
such as Wolff-Parkinson-White syndrome, as
should prior ECGs with delta waves, history
of an accessory pathway, or very young
patients with new-onset AF. Urgent electrical
Emergency Medicine Practice © 201320
cardioversion should be performed for
patients who are hemodynamically unstable
with AF/AFL involving conduction over an
accessory pathway, while IV procainamide,
ibutilide, or amiodarone may be considered for
hemodynamically stable patients.
4. “She was hypotensive, so I gave calcium
gluconate before giving the commonly quoted
starting dose of diltiazem: a 20-mg bolus. It
is unfortunate that she became profoundly
hypotensive and went into cardiac arrest, but I
did nothing wrong.”
Pretreatment with calcium may potentially
help blunt the hypotensive effects of diltiazem;
however, had you started with a lower
dose and titrated it slowly, you may have
been able to prevent the hypotension and
cardiac arrest. You can also consider using
vasopressors, cardioversion, or an amiodarone
drip to minimize hypotension and prevent
decompensation.
5. “When the diltiazem didn’t give a good response, I decided to try metoprolol. I believe
her complete heart block was from the acute
coronary syndrome she was having, not what I
did.”
Combining IV beta blockers and calcium
channel blockers can result in hypotension
and can precipitate dysrhythmia and complete
atrioventricular nodal blockade. It is safe to give
1 of these 2 classes of drugs intravenously—
cautiously—if the patient is on an oral version
of the other class, but giving both intravenously
in a short time period could potentially lead to
decompensation. www.ebmedicine.net • February 2013
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19. Stewart S. Epidemiology and economic impact of atrial
Risk Management Pitfalls For Atrial Fibrillation (continued from page 20)
6. “I thought the patient might be having acute
coronary syndrome, so I used a beta blocker
for its beneficial effects. I was not expecting
the patient to decompensate around that same
time.”
While there are advantages to using a beta
blocker in new-onset AF in the setting of acute
coronary syndromes or thyrotoxicosis, it is
important to remember any contraindications
to specific drug classes. Had you asked the
patient about a history of asthma and her recent
increased use of home nebulizers you might
have considered a short-acting beta blocker such
as esmolol or a calcium channel blocker instead.
usually occur in younger patients. A thyroidstimulating hormone screening is a reasonable
test in patients > 55 years of age with new-onset
AF.
9. “The patient was hypotensive, so I tried
cardioversion. I couldn’t get him to cardiovert
after multiple attempts with 200 J, so I gave
IV metoprolol to slow the heart rate down in
hopes that the decreased rate would improve
ventricular filling and increase his blood pressure. I couldn’t believe that it worsened his
blood pressure and he ended up going into
cardiac arrest.”
Failed cardioversion may occur in patients
with long-standing AF/AFL, and pretreatment
with an antiarrhythmic such as amiodarone
may decrease the defibrillation threshold
and improve success of cardioversion.
Atrioventricular nodal blocking agents may
slow the rate down, but this does not increase
the “atrial kick” contribution to ventricular
filling; thus, atrioventricular nodal blocking
agents will likely only exacerbate the
hypotension.
7. “Sure, her AF was 1 week old, but I obtained a
transesophageal echocardiogram that showed
no left atrial clot, so I cardioverted the patient and sent her home. She was just one of
those unfortunate people who had a thromboembolic event.”
Although there is some suggestion in the
literature that the method you used might be
reasonable, the data suggest that anticoagulation
would be required even with a negative
transesophageal echocardiogram in this
situation. If someone has been in AF for more
than 48 hours, transesophageal echocardiogram
may not show a clot, but there may still be as
high as a 2% incidence of thromboembolism
after conversion due to atrial stunning and
dysfunction after cardioversion.
10. “She was altered and couldn’t tell me how long
she had been in AF. I didn’t want to cardiovert
her and cause a stroke, so I gave diltiazem.”
The patient was showing evidence of poor
perfusion with altered mental status, cool,
clammy skin, and hypotension, and she needed
immediate electrical cardioversion. Heparin
should be started as soon as possible after
cardioversion unless there is a significant
contraindication.
8. “She didn’t look bug-eyed to me.”
In the elderly, thyrotoxicosis can present very
atypically, without the common findings that
February 2013 • www.ebmedicine.net
21
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control in atrial fibrillation. Am J Cardiol. 1992;69(7):36B-40B.
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118. Ellenbogen KA, Dias VC, Cardello FP, et al. Safety and efficacy of intravenous diltiazem in atrial fibrillation or atrial
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120. Phillips BG, Gandhi AJ, Sanoski CA, et al. Comparison of
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121. Salerno DM, Dias VC, Kleiger RE, et al. Efficacy and safety
of intravenous diltiazem for treatment of atrial fibrillation
and atrial flutter. The diltiazem-atrial fibrillation/flutter
study group. Am J Cardiol. 1989;63(15):1046-1051. (Prospective multicenter randomized placebo-controlled trial; 113
patients)
122. Elam K, Bolar-Softich KL. Dilemmas in the acute pharmacologic treatment of uncontrolled atrial fibrillation. Am J Emerg
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123. Olshansky B. Management of atrial fibrillation after coronary
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124. Lip GY, Tse HF. Management of atrial fibrillation. Lancet.
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125. Siu CW, Lau CP, Lee WL, et al. Intravenous diltiazem is
superior to intravenous amiodarone or digoxin for achieving
ventricular rate control in patients with acute uncomplicated
atrial fibrillation. Crit Care Med. 2009;37(7):2174-2179. (Prospective randomized controlled trial; 150 patients)
126. Sarter BH, Marchlinski FE. Redefining the role of digoxin in the treatment of atrial fibrillation. Am J Cardiol.
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127. Jacob S, Ali OA, Pidlaoan V, et al. Pharmacotherapy of atrial
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128. Rienstra M, Van Gelder IC. Who, when and how to rate control for atrial fibrillation. Curr Opin Cardiol. 2008;23(1):23-27.
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129. Cheng JW, Rybak I. Use of digoxin for heart failure and atrial
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130. Lewis RV, Laing E, Moreland TA, et al. A comparison of
digoxin, diltiazem and their combination in the treatment of
atrial fibrillation. Eur Heart J. 1988;9(3):279-283. (Prospective
randomized double-blind crossover study; 14 patients)
131. Parris RJ, Clarke SF. Towards evidence based emergency
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treatment of recent-onset atrial fibrillation: results of a randomized, controlled study. J Am Coll Cardiol. 1996;27(5):10791082. (Prospective randomized controlled trial; 100
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134. Chevalier P, Durand-Dubief A, Burri H, et al. Amiodarone
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2003;41(2):255-262. (Meta-analysis; 13 studies, 1174 patients)
135. Hou ZY, Chang MS, Chen CY, et al. Acute treatment of
recent-onset atrial fibrillation and flutter with a tailored
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136. Brodsky MA, Orlov MV, Capparelli EV, et al. Magnesium therapy in new-onset atrial fibrillation. Am J Cardiol.
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137. Chiladakis JA, Stathopoulos C, Davlouros P, et al. Intravenous magnesium sulfate versus diltiazem in paroxysmal
atrial fibrillation. Int J Cardiol. 2001;79(2-3):287-291. (Prospective randomized trial; 46 patients)
138. Chu K, Evans R, Emerson G, et al. Magnesium sulfate versus
placebo for paroxysmal atrial fibrillation: a randomized clinical trial. Acad Emerg Med. 2009;16(4):295-300. (Prospective
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139. Gullestad L, Birkeland K, Molstad P, et al. The effect of magnesium versus verapamil on supraventricular arrhythmias.
Clin Cardiol. 1993;16(5):429-434. (Prospective single-blind
study; 15 patients)
140. Hays JV, Gilman JK, Rubal BJ. Effect of magnesium sulfate
on ventricular rate control in atrial fibrillation. Ann Emerg
Med. 1994;24(1):61-64. (Randomized prospective doubleblind placebo-controlled study; 15 patients)
141. Moran JL, Gallagher J, Peake SL, et al. Parenteral magnesium
sulfate versus amiodarone in the therapy of atrial tachyarrhythmias: a prospective, randomized study. Crit Care Med.
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February 2013 • www.ebmedicine.net
142. Simonian SM, Lotfipour S, Wall C, et al. Challenging the superiority of amiodarone for rate control in Wolff-ParkinsonWhite and atrial fibrillation. Intern Emerg Med. 2010;5(5):421426. (Review)
143. Falcone RA, Morady F, Armstrong WF. Transesophageal
echocardiographic evaluation of left atrial appendage function and spontaneous contrast formation after chemical or
electrical cardioversion of atrial fibrillation. Am J Cardiol.
1996;78(4):435-439. (Case series; 23 patients)
144. Weigner MJ, Caulfield TA, Danias PG, et al. Risk for clinical thromboembolism associated with conversion to sinus
rhythm in patients with atrial fibrillation lasting less than
48 hours. Ann Intern Med. 1997;126(8):615-620. (Prospective
study; 1822 patients)
145. Gage BF, Cardinalli AB, Owens DK. Cost-effectiveness of
preference-based antithrombotic therapy for patients with
nonvalvular atrial fibrillation. Stroke. 1998;29(6):1083-1091.
(Cost/decision analysis)
146. Hart RG, Benavente O, McBride R, et al. Antithrombotic
therapy to prevent stroke in patients with atrial fibrillation:
a meta-analysis. Ann Intern Med. 1999;131(7):492-501. (Metaanalysis; 16 trials, 9874 patients)
147. Lip GY, Lim HS. Atrial fibrillation and stroke prevention.
Lancet Neurol. 2007;6(11):981-993. (Review)
148. ACTIVE Investigators, Connolly SJ, Pogue J, et al. Effect of
clopidogrel added to aspirin in patients with atrial fibrillation. N Engl J Med. 2009;360(20):2066-2078. (Randomized
double blind multicenter trial; 7554 patients)
149. ACTIVE Writing Group of the ACTIVE Investigators, Connolly S, Pogue J, et al. Clopidogrel plus aspirin versus oral
anticoagulation for atrial fibrillation in the atrial fibrillation
clopidogrel trial with irbesartan for prevention of vascular
events (ACTIVE W): a randomised controlled trial. Lancet.
2006;367(9526):1903-1912. (Randomized double blind multicenter trial; 3371 patients)
150. Aguilar MI, Hart R, Pearce LA. Oral anticoagulants versus
antiplatelet therapy for preventing stroke in patients with
non-valvular atrial fibrillation and no history of stroke
or transient ischemic attacks. Cochrane Database Syst Rev.
2007;(3)(3):CD006186. (Systematic review and meta-analysis; 9598 patients)
151. Patel MR, Mahaffey KW, Garg J, et al. Rivaroxaban versus
warfarin in nonvalvular atrial fibrillation. N Engl J Med.
2011;365(10):883-891. (Randomized double-blind trial;
14,264 patients)
152. Nagarakanti R, Ezekowitz MD, Oldgren J, et al. Dabigatran
versus warfarin in patients with atrial fibrillation: an analysis of
patients undergoing cardioversion. Circulation. 2011;123(2):131136. (Prospective randomized study; 1270 patients)
153. Granger CB, Alexander JH, McMurray JJ, et al. Apixaban
versus warfarin in patients with atrial fibrillation. N Engl J
Med. 2011;365(11):981-992. (Randomized double-blind trial;
1201 patients)
154. Davis EM, Packard KA, Knezevich JT, et al. New and emerging anticoagulant therapy for atrial fibrillation and acute
coronary syndrome. Pharmacotherapy. 2011;31(10):975-1016.
(Review)
155. De Caterina R, Husted S, Wallentin L, et al. New oral anticoagulants in atrial fibrillation and acute coronary syndromes:
ESC Working Group on Thrombosis-Task Force on Anticoagulants in Heart Disease position paper. J Am Coll Cardiol.
2012;59(16):1413-1425. (Review)
156.*Lip GY, Larsen TB, Skjoth F, et al. Indirect comparisons of
new oral anticoagulant drugs for efficacy and safety when
used for stroke prevention in atrial fibrillation. J Am Coll
Cardiol. 2012;60(8):738-746. (Phase III clinical trial review)
157. Paikin JS, Haroun MJ, Eikelboom JW. Dabigatran for stroke
prevention in atrial fibrillation: the RE-LY trial. Expert Rev
Cardiovasc Ther. 2011;9(3):279-286. (Randomized multicenter
clinical trial; 18,113 patients)
25
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158. Shah SV, Gage BF. Cost-effectiveness of dabigatran
for stroke prophylaxis in atrial fibrillation. Circulation.
2011;123(22):2562-2570. (Trial review)
159. Gage BF, Waterman AD, Shannon W, et al. Validation of
clinical classification schemes for predicting stroke. Results
from the National Registry of Atrial Fibrillation. JAMA.
2001;285(22):2864-2870.
160. Keogh C, Wallace E, Dillon C, et al. Validation of the
CHADS2 clinical prediction rule to predict ischaemic stroke.
A systematic review and meta-analysis. Thromb Haemost.
2011;106(3):528-538. (Meta-analysis; 2815 patients, 8 databases)
161. Poli D, Lip GY, Antonucci E, et al. Stroke risk stratification in
a “real-world” elderly anticoagulated atrial fibrillation population. J Cardiovasc Electrophysiol. 2011;22(1):25-30. (Prospective study; 662 patients)
162. Lip GY, Nieuwlaat R, Pisters R, et al. Refining clinical risk
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in atrial fibrillation using a novel risk factor-based approach: the Euro heart survey on atrial fibrillation. Chest.
2010;137(2):263-272. (Comparative study; 1577 patients)
163.*Olesen JB, Torp-Pedersen C, Hansen ML, et al. The value of
the CHA2DS2-VASc score for refining stroke risk stratification in patients with atrial fibrillation with a CHADS2
score 0-1: a nationwide cohort study. Thromb Haemost.
2012;107(6):1172-1179. (Registry review; 47,576 patients)
164. Larsen TB, Lip GY, Skjoth F, et al. Added predictive ability
of the CHA2DS2VASc risk score for stroke and death in
patients with atrial fibrillation: the prospective Danish diet,
cancer, and health cohort study. Circ Cardiovasc Qual Outcomes. 2012;5(3):335-342. (Retrospective review of prospective cohort study; 1603 patients)
165. Cha MJ, Kim YD, Nam HS, et al. Stroke mechanism in
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the CHADS2 and CHA2 DS2 -VASc scores. Eur J Neurol.
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166. Boriani G, Botto GL, Padeletti L, et al. Improving stroke
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risk scores in patients with paroxysmal atrial fibrillation
by continuous arrhythmia burden monitoring. Stroke.
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and thromboembolic risk: what is the extent of adherence to guidelines in clinical practice? Rev Port Cardiol.
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169. Brophy MT, Snyder KE, Gaehde S, et al. Anticoagulant
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170. Marinigh R, Lip GY, Fiotti N, et al. Age as a risk factor for
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171. Ruiz Ortiz M, Romo Penas E, Franco Zapata MF, et al. Oral
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174. Douketis JD, Arneklev K, Goldhaber SZ, et al. Comparison of
Emergency Medicine Practice © 201326
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(Pooled analysis; 7329 patients)
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www.ebmedicine.net • February 2013
6. For a patient with Wolff-Parkinson-White preexcitation syndrome, which of the following
medication is safest to use?
a. Esmolol
b. Diltiazem
c. Magnesium
d. Procainamide
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7. Routine transthoracic echocardiography should
be performed on every patient who presents to
the ED with new-onset AF.
a. True b. False 8. Failed electrical cardioversion is associated
with:
a. Thyrotoxicosis
b. Long-standing AF
c. Dilated left atrium
d. All of the above
9. Which of these agents has shown to be the fastest at achieving rate control?
a. Amiodarone
b. Esmolol
c. Digoxin
d. Metoprolol
1. In AF, the P-wave:
a. Is absent
b. Is buried in the QRS complex
c. Precedes every QRS complex
d. Has a sawtooth pattern
2. AFL is characterized by:
a. Irregularly irregular ventricular rhythm
b. Atrial rate of 250-350 beats/min
c. Absent P-wave
d. Ventricular rate between 180 and 250 beats/
min
10. Which of the following is the most likely
explanation for a thromboembolic event after
cardioversion?
a. Failure to detect a left atrial clot on transesophageal echocardiogram performed before cardioversion
b. Atrial “stunning” and mechanical dysfunction following electrical cardioversion
c. Dabigatran, which is inferior to warfarin in preventing thromboembolic events, was given prior to cardioversion
3. All patients who are hemodynamically unstable and in AF should be immediately cardioverted.
a. True
b. False
4. Strategies to rate control hypotensive patients in rapid AF include all of the following EXCEPT:
a. Pretreatment with calcium gluconate
b. 20 mL/kg crystalloid bolus infusion
c. Diltiazem 2.5 mg/min continuous drip until heart rate < 100 beats/min or 50 mg total dose
d. Diltiazem 3 mg/kg IV push
Save The Date!
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In Emergency Medicine conference
is back! Mark your calendars for
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5. Nondihydropyridine calcium channel blockers such as diltiazem and verapamil are firstline rate control medications for patients with
which of the following conditions?
a. Thyrotoxicosis
b. Asthma exacerbation
c. Congestive heart failure
d. Contraindication to beta blockers
February 2013 • www.ebmedicine.net
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